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The Amyotrophic Lateral Sclerosis-Parkinsonism-Dementia Complex of Guam

Barry J. Snow, FRACP; Richard F. Peppard, FRACP; Mark Guttman, FRCPC; Junichi Okada, MD; W. R. Wayne Martin, FRCPC; John Steele, FRCPC; Andrew Eisen, FRCPC; Geoffrey Carr, PhD; Bruce Schoenberg, MD; Donald Calne, FRCPC

Arch Neurol. 1990;47(8):870-874.

Abstract
• We performed positron emission tomography using ¹⁸F-6-fluorodopa on four Guamanians with an amyotrophic lateral sclerosis syndrome, eight Guamanians with parkinsonism, and seven clinically normal Guamanians; the results were compared with those of nine Vancouver control subjects. The Guamanian subjects had all been exposed to similar Chamorro life-styles. The scans were analyzed using a graphic method that calculates a constant for whole striatal ¹⁸F-6-fluorodopa uptake. The parkinsonian subjects all had significantly reduced striatal ¹⁸F-6-fluorodopa uptake. The group with amyotrophic lateral sclerosis had significantly reduced uptake that was intermediate between that of the control group and the parkinsonian group. Two Guamanian normal subjects had reduced striatal ¹⁸F-6-fluorodopa uptake. The nigrostriatal dopaminergic lesion in Guamanian parkinsonism is similar to that found in idiopathic parkinsonism. The nigrostriatal lesions in the subjects with amyotrophic lateral sclerosis and the Guamanian normal subjects are examples of subclinical neuronal damage demonstrable in living subjects with positron emission tomography.

Author Affiliations
From the Belzberg Laboratory of Clinical Neurosciences, Division of Neurology, University of British Columbia, Vancouver (Drs Snow, Peppard, Guttman, Okada, Martin, Eisen, Carr, Schoenberg, and Calne); and Guam Memorial Hospital, Taumuning (Dr Steele).; Deceased.

Footnotes
Accepted for publication December 18, 1989.

Reprints not available.

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